Other recurring genomic rearrangements involve the genes PTEN and MAGI2. PTEN is a well-known tumor suppressor gene and MAGI2 appears to be its helpmate; mutations to one or both genes may set cells on the path toward becoming cancerous. Drugs that inhibit the pathway these genes influence are also being developed, raising the possibility that the drugs could be applied to prostate cancer.
In addition to uncovering new and suspected genes, whole genome sequencing has also given Drs. Garraway, Rubin and their colleagues insights into how genomic rearrangements arise in the first place. With a catalog of rearrangements in hand, the researchers looked for where breaks and reattachments tended to occur and found that these events are not distributed randomly across the genome. Rather, in some tumors these events tend to take place in areas of the genome that are inactive or silent, while in other tumors they occur in regions that are highly active. This pattern suggests that mistakes made by cells while turning genes on and off might give rise to DNA rearrangements and therefore play a formative role in cancer's development.
The researchers' findings may also provide a key starting point for the development of new diagnostic tools for prostate cancer. Currently, when patients are diagnosed with prostate cancer, it is almost impossible for doctors to determine if the disease will advance quickly and therefore require aggressive treatment, or whether the tumors will remain slow-growing, necessitating a wait-and-see approach. "This study could enhance our ability to develop new, diagnostic markers for prostate c
|Contact: Andrew Klein|
New York- Presbyterian Hospital/Weill Cornell Medical Center/Weill Cornell Medical College